Clinical assesment of ventricular ejection dynamics with and without outflow obstruction

We evaluated the ability of Doppler echocardiography to assess left ventricular performance in six open-chest dogs studied under various conditions. Intravenous infusions of nitroglycerin were used to vary preload, atrial pacing was used to control heart rate, and changes in inotropic state were induced by two different doses of dobutamine (5 and 10 micrograms/kg/min iv) and by administration of propranolol (1 mg/kg iv). Left ventricular anterior wall myocardial segment length was used as an index of preload. Maximum aortic blood flow, peak acceleration of aortic blood flow, and dP/dt were measured with an electromagnetic flow probe around the ascending aorta and a high-fidelity pressure transducer in the left ventricle. A continuous-wave Doppler transducer applied to the aortic arch was used to measure peak aortic blood velocity, mean acceleration, time to peak velocity, and the systolic velocity integral. The differences between mean values obtained under different inotropic conditions were significant at the p less than .01 level for peak velocity and at the p less than .05 level for mean acceleration. Within a given animal, Doppler measurements of peak velocity correlated very closely with maximum aortic flow (r = .96), maximum acceleration of aortic flow (r = .95), and with maximum dP/dt (r = .92). Mean acceleration measured by Doppler echocardiography also correlated very closely with conventional indexes, but was subject to greater interobserver variability. Doppler measurements of time to peak and the systolic velocity integral correlated less well with conventional hemodynamic indexes.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of preload and heart rate on Doppler echocardiographic indexes of left ventricular performance: comparison with invasive indexes in an experimental preparation.

In this study we introduce a new concept of systolic myocardial stiffness that extends the Suga-Sagawa maximum ventricular elastance concept to the myocardium. End-systole is defined as the time of maximum systolic myocardial stiffness (max Eav), which we examined for its load independence and sensitivity to changes in the inotropic state and to heart rate. Seven adult mongrel dogs were instrumented with ultrasonic crystals for measurements of long and short axes and left ventricular wall thickness, and a high-fidelity micromanometer was inserted for measurement of left ventricular pressures. Preload and afterload were altered by inferior vena cava occlusion, nitroprusside, angiotensin II, atropine, propranolol, and various combinations with propranolol. End-systolic stress-strain relations (slope: max Eav) were linear in all seven dogs, implying that end-systolic myocardial stiffness is independent of end-systolic stress. Changes in max Eav (for constant preload and afterload) reflected changes in the ejection fraction; max Eav was also insensitive to propranolol and to changes in heart rate over the range from 120 to 180 beats/min. End-systolic pressure-volume relations (ESPVRs), derived analytically from these stress-strain relations, were nonlinear, and estimates of volume at zero stress (Vom) were always positive. On the other hand, ESPVRs obtained on the basis of the Suga-Sagawa maximum ventricular elastance concept, were linear, and volume at zero pressure (Vop) estimated by linear extrapolation was negative in one case. Based on the concept of systolic myocardial stiffness, the slope of the ESPVR varies with end-systolic volume and attains its maximum value (Emax) at zero end-systolic pressure. Normalization of Emax with Vom demonstrated a close relationship to max Eav. Thus both max Eav and Vom and Emax are ideal variables for assessing changes in myocardial contractility when preload and afterload are constant. Furthermore, Vom and max Eav permit development of the entire ejection fraction-afterload relationship for a given preload, thus providing a method for comparing myocardial contractile states between ventricles.

The development of the entire end-systolic pressure-volume and ejection fraction-afterload relations: a new concept of systolic myocardial stiffness.

We used a cryosurgical technique to ablate the atrioventricular (AV) node-His bundle in twenty-two selected patients with disabling supraventricular tachyarrhythmias unresponsive to medical management. Successful AV block was achieved in seventeen. There was no intraoperative mortality and significant surgical complications were not encountered. Electrophysiologic studies performed 7-10 days after surgery revealed that the subsidiary pacemaker had a narrow QRS complex morphology and a mean cycle length of 1244 msec. Isoproterenol (1-4 microgram/min i.v.) significantly increased (p less than 0.01) the rate of the subsidiary pacemaker (mean maximum response 1008.3 msec); atropine (2 mg i.v.) had no effect on its rate. The cycle length of the subsidiary pacemaker during long-term follow-up (mean 14.8 months) showed a small but significant (p = 0.024) increase (mean cycle length 1430 msec). Treadmill exercise in seven patients did not result in the subsidiary pacemaker exceeding the rate of the implanted demand pacemaker set at 70 beats/min. The properties of the subsidiary pacemaker suggest an intra-Hisian site of impulse formation.

Cryosurgical ablation of the atrioventricular node-His bundle: long-term follow-up and properties of the junctional pacemaker.

Doppler echocardiography was used to measure stroke volume, peak flow velocity, and acceleration of flow in the ascending aorta in 10 healthy young volunteers during unlimited supine bicycle exercise and upright treadmill exercise. High quality studies were obtained in all subjects through the suprasternal notch acoustic window; there was no appreciable degradation in Doppler signal caused by interference by increased respiration or chest wall motion. Stroke volume index increased from 54 ml/m2 at rest to 63.5 ml/m2 at peak supine exercise and from 38 ml/m2 standing at rest to 63.3 ml/m2 during peak upright exercise. Mean peak flow velocity rose from 0.91 m/s at supine rest to 1.36 m/s during maximum supine exercise. In the upright position mean peak flow velocity increased from 0.75 m/s at rest to 1.39 m/s during maximum exercise. Mean peak velocities were lower in the upright position at rest but were not significantly different at peak exercise. Mean acceleration of flow in the ascending aorta increased from 12.02 m/s2 during supine rest to 21.6 m/s2 during supine exercise and from 10.8 m/s2 at rest on the treadmill to 21.9 m/s2 during peak upright exercise. This study shows that echocardiographic measurement of ascending aortic blood flow by the Doppler technique is feasible even during vigorous exercise; that stroke volume and peak flow velocity at rest are lower in the upright position than in the supine position but equalise at peak exercise; and that acceleration of flow in the ascending aorta is the same in both the supine and upright positions and increases equally at peak exercise in both positions.

https://heart.bmj.com/content/heartjnl/54/6/562.full.pdf

Doppler echocardiographic measurement of flow velocity in the ascending aorta during supine and upright exercise.

A catheter-tip velocity transducer with two high-fidelity pressure manometers was used to evaluate the left ventricular (LV) hemodynamic effects of intravenous propranolol (10 mg). Nine patients without clinical evidence of heart failure were studied. Pulsatile ascending aortic blood flow velocity and pressure and LV pressure were measured continuously during drug administration. Beat-to-beat changes in stroke volume index, stroke work index, LV end-diastolic pressure, maximum blood flow velocity and acceleration, and maximum LV dP/dt were determined. Propranolol produced a decrease in maximum blood flow velocity (from 58 +/- 4.7 to 42 +/- 5.1 cm/sec, p less than 0.002), and acceleration (from 1181 +/- 130 to 847 +/- 117 cm/sec2, p less than 0.002, max dP/dt (from 1361 +/- 70 to 1146 +/- 63 mm Hg/sec, p less than 0.002), stroke volume index (from 47 +/- 3.0 to 38 +/- 3.2 ml/m2, p less than 0.002) and total stroke work index (from 702 +/- 33 to 603 +/- 44 mJ/m2 p less than 0.04), with little change in mean aortic pressure, peak systolic pressure and LV end-diastolic pressure. Depression in myocardial function was detectable within 1 minute after initiation of propranolol and persisted when negative chronotropic effects were eliminated by atrial pacing. The multisensor catheter technique allows rapid and safe detection of changes in cardiovascular function during propranolol administration in conscious man.

M E Ray

Papers

Use of catheter-tip velocity--pressure transducer to evaluate left ventricular function in man: effects of intravenous propranolol.